Kidney Week

Abstract: FR-PO596

SPECT/CT with Technetium 99m-Methyl Diphosphonate for the Diagnosis of Severe Symptomatic Hypercalcemia After Rhabdomyolysis Induced AKI in 2 Patients with Cirrhosis

Session Information

• Trainee Case Reports - III
  October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

• 902 Fluid and Electrolytes: Clinical

Authors

• Ramirez, Silvia, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Mexico City, Mexico

Silvia Ramirez,

• Gómez Ruiz, Ismael Antonio, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico

Ismael Antonio Gómez Ruiz,

• Cohen-Bucay, Abraham, Boston University Medical Center, Boston, Massachusetts, United States

Abraham Cohen-Bucay,

• Correa-Rotter, Ricardo, Institutor Nacional de la Nutricion, Mexico City, Mexico

Ricardo Correa-Rotter,

Introduction

Rhabdomyolysis induced acute kidney injury (RI-AKI) is often complicated by multiple electrolyte abnormalities. Hypercalcemia (HC) due to soft tissue mobilization of calcium deposits in the recovery phase of RI-AKI has been described yet severe HC is rare. We present two patients with cirrhosis who developed RI-AKI and severe HC, both with SPECT/CT deposit images

Case Description

Case 1: 56-yr-old female, primary biliary cholangitis Child-Pugh B cirrhosis who developed exertional RI-AKI that required hemodialysis (HD). She was hypocalcemic during the oliguric phase; during the recovery phase developed severe HC (peak of 16.2 mg/dl) with neurological symptoms. She required intermittent 13 sessions of HD in addition to volume replacement, diphosphonates, and diuretics and recovered in 8 weeks. Plasma levels of 25-OH and 1-25(OH)2 vitamin D were low, iPTH appropriately suppressed. A SPECT/CT with ⁹⁹Tc^m-methyl diphosphonate (⁹⁹Tc^m-MDP) demonstrated extensive soft tissue tracer accumulation (Fig1). Case 2: 65-yr-old female, Child-Pugh B cirrhosis secondary to hepatitis C, who developed exertional RI-AKI that required HD. Normocalcemic during the oliguric phase yet during the recovery phase developed severe symptomatic HC (peak 14.7 mg/dl), requiring 3 intermittent HD sessions. HC lasted for 2 weeks. Plasma levels of 25-OH and 1-25(OH) vitamin D were low, iPTH level appropriately suppressed and a SPECT/CT with ⁹⁹Tc^m-MDP demonstrated soft tissue tracer accumulation. The evolution of serum calcium, phosphorus, and creatinine levels are showed in Fig1. Both patients had full renal and neurological recovery.

Discussion

SPECT/CT with ⁹⁹Tc^m-MDP is a useful tool to identify soft tissue calcium deposits in patients with HC after RI-AKI. Intermittent HD is an effective treatment for severe HC. Since both of our patients were cirrhotic, we postulate that cirrhosis might be a risk factor for HC during the recovery phase of RI-AKI.